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eightopals · 2 years ago

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So my cardiac blockages have never got so far as to cause a heart attack. I have had 3 angioplasties and now have 2 cardiac stents.

I had my first incident at age 31, more than 30 years ago (yes, I’m old). I was fairly active, walking and practicing Aikido. I started getting what felt like indigestion. It seemed to happen when I was out walking.

I went to 2 pool parties on Labor Day Weekend that year. At both, as was my habit, I towed little kids around the pool on floats. It’s strenuous. I had the indigestion thing worse than ever …and I noticed it was in time with my pulse.

I took myself to the hospital on the Monday holiday. I had the damnedest time getting them to consider the idea of a heart problem. One young cardiologist supported me. He said my family history was compelling (both my parents had multiple angioplasties at the dawn of the use of this technique).

It turned I had a 95% or greater blockage of the left anterior descending (LAD) artery of the heart. The LAD is the “widow maker” because a complete blockage will kill you in no time.

The next two times it happened were 6 years ago and last September. I called the office of my cardiologist - the same cardiologist - and they took me right away, did imaging, and put me in the hospital for a stent.

KNOW YOUR BODY. Pay attention to what it’s telling you. Don’t take no for an answer.

A nurse has heart attack and describes what she felt like when having one

I am an ER nurse and this is the best description of this event that I have ever heard.

FEMALE HEART ATTACKS

I was aware that female heart attacks are different, but this is description is so incredibly visceral that I feel like I have an entire new understanding of what it feels like to be living the symptoms on the inside. Women rarely have the same dramatic symptoms that men have… you know, the sudden stabbing pain in the chest, the cold sweat, grabbing the chest & dropping to the floor the we see in movies. Here is the story of one woman’s experience with a heart attack:

"I had a heart attack at about 10:30 PM with NO prior exertion, NO prior emotional trauma that one would suspect might have brought it on. I was sitting all snugly & warm on a cold evening, with my purring cat in my lap, reading an interesting story my friend had sent me, and actually thinking, ‘A-A-h, this is the life, all cozy and warm in my soft, cushy Lazy Boy with my feet propped up. A moment later, I felt that awful sensation of indigestion, when you’ve been in a hurry and grabbed a bite of sandwich and washed it down with a dash of water, and that hurried bite seems to feel like you’ve swallowed a golf ball going down the esophagus in slow motion and it is most uncomfortable. You realize you shouldn’t have gulped it down so fast and needed to chew it more thoroughly and this time drink a glass of water to hasten its progress down to the stomach. This was my initial sensation–the only trouble was that I hadn’t taken a bite of anything since about 5:00 p.m.

After it seemed to subside, the next sensation was like little squeezing motions that seemed to be racing up my SPINE (hind-sight, it was probably my aorta spasms), gaining speed as they continued racing up and under my sternum (breast bone, where one presses rhythmically when administering CPR). This fascinating process continued on into my throat and branched out into both jaws. ‘AHA!! NOW I stopped puzzling about what was happening – we all have read and/or heard about pain in the jaws being one of the signals of an MI happening, haven’t we? I said aloud to myself and the cat, Dear God, I think I’m having a heart attack! I lowered the foot rest dumping the cat from my lap, started to take a step and fell on the floor instead. I thought to myself, If this is a heart attack, I shouldn’t be walking into the next room where the phone is or anywhere else… but, on the other hand, if I don’t, nobody will know that I need help, and if I wait any longer I may not be able to get up in a moment.

I pulled myself up with the arms of the chair, walked slowly into the next room and dialed the Paramedics… I told her I thought I was having a heart attack due to the pressure building under the sternum and radiating into my jaws. I didn’t feel hysterical or afraid, just stating the facts. She said she was sending the Paramedics over immediately, asked if the front door was near to me, and if so, to un-bolt the door and then lie down on the floor where they could see me when they came in. I unlocked the door and then laid down on the floor as instructed and lost consciousness, as I don’t remember the medics coming in, their examination, lifting me onto a gurney or getting me into their ambulance, or hearing the call they made to St. Jude ER on the way, but I did briefly awaken when we arrived and saw that the radiologist was already there in his surgical blues and cap, helping the medics pull my stretcher out of the ambulance. He was bending over me asking questions (probably something like ‘Have you taken any medications?’) but I couldn’t make my mind interpret what he was saying, or form an answer, and nodded off again, not waking up until the Cardiologist and partner had already threaded the teeny angiogram balloon up my femoral artery into the aorta and into my heart where they installed 2 side by side stints to hold open my right coronary artery.

I know it sounds like all my thinking and actions at home must have taken at least 20-30 minutes before calling the paramedics, but actually it took perhaps 4-5 minutes before the call, and both the fire station and St Jude are only minutes away from my home, and my Cardiologist was already to go to the OR in his scrubs and get going on restarting my heart (which had stopped somewhere between my arrival and the procedure) and installing the stents. Why have I written all of this to you with so much detail? Because I want all of you who are so important in my life to know what I learned first hand.

1. Be aware that something very different is happening in your body, not the usual men’s symptoms but inexplicable things happening (until my sternum and jaws got into the act). It is said that many more women than men die of their first (and last) MI because they didn’t know they were having one and commonly mistake it as indigestion, take some Maalox or other anti-heartburn preparation and go to bed, hoping they’ll feel better in the morning when they wake up… which doesn’t happen. My female friends, your symptoms might not be exactly like mine, so I advise you to call the Paramedics if ANYTHING is unpleasantly happening that you’ve not felt before. It is better to have a ‘false alarm’ visitation than to risk your life guessing what it might be! 2. Note that I said ‘Call the Paramedics.’ And if you can take an aspirin. Ladies, TIME IS OF THE ESSENCE! Do NOT try to drive yourself to the ER - you are a hazard to others on the road. Do NOT have your panicked husband who will be speeding and looking anxiously at what’s happening with you instead of the road. Do NOT call your doctor – he doesn’t know where you live and if it’s at night you won’t reach him anyway, and if it’s daytime, his assistants (or answering service) will tell you to call the Paramedics. He doesn’t carry the equipment in his car that you need to be saved! The Paramedics do, principally OXYGEN that you need ASAP. Your Dr. will be notified later. 3. Don’t assume it couldn’t be a heart attack because you have a normal cholesterol count. Research has discovered that a cholesterol elevated reading is rarely the cause of an MI (unless it’s unbelievably high and/or accompanied by high blood pressure). MIs are usually caused by long-term stress and inflammation in the body, which dumps all sorts of deadly hormones into your system to sludge things up in there. Pain in the jaw can wake you from a sound sleep. Let’s be careful and be aware. The more we know the better chance we could survive to tell the tale.“

Reblog, repost, Facebook, tweet, pin, email, morse code, fucking carrier pigeon this to save a life! I wish I knew who the author was. I’m definitely not the OP, actually think it might be an old chain email or even letter from back in the day. The version I saw floating around Facebook ended with “my cardiologist says mail this to 10 friends, maybe you’ll save one!” And knew this was way too interesting not to pass on.

#health #heart #heart attack in women #cardiology #nurse #emt #nurblr #nurseblr #medicine #emergency #heart attack

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rnedicalimaging · 7 months ago

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14th May 2024

Yale: Introduction to Radiology - Abdominal Anatomy on Computed Tomography

youtube

Abdominal Anatomy on Computed Tomography - Learning Objective:

Identify the normal appearance of the following organs:

spleen, adrenal glands, kidneys, gallbladder, pancreas, liver, stomach, duodenum, colon (ascending, transverse, descending)

Identify the following venous structures:

IVC, hepatic veins, portal vein, splenic vein

Identify the following arteries

aorta, celiac artery, common hepatic artery, splenic artery, left gastric artery, superior mesenteric artery, renal artery, inferior mesenteric artery

Most abdominal CT scans are performed at about 70 seconds after giving intravenous contrast.

Sometimes, imaging is earlier for interest in the arteries.

Sometimes, imaging is later in certain specific pathology.

PA vs AP:

You know you're posterior because you can see the lumbar spine and thorasic soine vertebrae bodies coming into the image

As you start to scroll towards anterior, you can see the abdominal aorta.

#Youtube

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skidoodle-doo · 11 months ago

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The pancreas is an organ of the digestive system and endocrine system of vertebrates. In humans, it is located in the abdomen behind the stomach and functions as a gland. The pancreas is a mixed or heterocrine gland, i.e., it has both an endocrine and a digestive exocrine function.[2] 99% of the pancreas is exocrine and 1% is endocrine.[3][4][5][6] As an endocrine gland, it functions mostly to regulate blood sugar levels, secreting the hormones insulin, glucagon, somatostatin and pancreatic polypeptide. As a part of the digestive system, it functions as an exocrine gland secreting pancreatic juice into the duodenum through the pancreatic duct. This juice contains bicarbonate, which neutralizes acid entering the duodenum from the stomach; and digestive enzymes, which break down carbohydrates, proteins and fats in food entering the duodenum from the stomach.

Pancreas

Anatomy of the pancreas

Details

Pronunciation

/ˈpæŋkriəs/

Precursor

Pancreatic buds

System

Digestive system and endocrine system

Artery

Inferior pancreaticoduodenal artery, anterior superior pancreaticoduodenal artery, posterior superior pancreaticoduodenal artery, splenic artery

Vein

Pancreaticoduodenal veins, pancreatic veins

Nerve

Pancreatic plexus, celiac ganglia, vagus nerve[1]

Lymph

Splenic lymph nodes, celiac lymph nodes and superior mesenteric lymph nodes

Identifiers

Latin

pancreas

Greek

Πάνκρεας (Pánkreas)

MeSH

D010179

TA98

A05.9.01.001

TA2

3114

FMA

7198

Anatomical terminology

[edit on Wikidata]

Inflammation of the pancreas is known as pancreatitis, with common causes including chronic alcohol use and gallstones. Because of its role in the regulation of blood sugar, the pancreas is also a key organ in diabetes mellitus. Pancreatic cancer can arise following chronic pancreatitis or due to other reasons, and carries a very poor prognosis, as it is often only identified after it has spread to other areas of the body.

The word pancreas comes from the Greek πᾶν (pân, "all") & κρέας (kréas, "flesh"). The function of the pancreas in diabetes has been known since at least 1889, with its role in insulin production identified in 1921.

Structure

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The pancreas (shown here in pink) sits behind the stomach, with the body near the curvature of the duodenum, and the tail stretching to touch the spleen.

The pancreas is an organ that in humans lies in the abdomen, stretching from behind the stomach to the left upper abdomen near the spleen. In adults, it is about 12–15 centimetres (4.7–5.9 in) long, lobulated, and salmon-coloured in appearance.[7]

Anatomically, the pancreas is divided into a head, neck, body, and tail. The pancreas stretches from the inner curvature of the duodenum, where the head surrounds two blood vessels: the superior mesenteric artery and vein. The longest part of the pancreas, the body, stretches across behind the stomach, and the tail of the pancreas ends adjacent to the spleen.[7]

Two ducts, the main pancreatic duct and a smaller accessory pancreatic duct run through the body of the pancreas. The main pancreatic duct joins with the common bile duct forming a small ballooning called the ampulla of Vater (hepatopancreatic ampulla). This ampulla is surrounded by a muscle, the sphincter of Oddi. This ampulla opens into the descending part of the duodenum. The opening of the common bile duct into main pancreatic duct is controlled by sphincter of Boyden. The accessory pancreatic duct opens into duodenum with separate openings located above the opening of the main pancreatic duct.[7]

Parts

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The head of the pancreas sits within the curvature of the duodenum, and wraps around the superior mesenteric artery and vein. To the right sits the descending part of the duodenum, and between these travel the superior and inferior pancreaticoduodenal arteries. Behind rests the inferior vena cava, and the common bile duct. In front sits the peritoneal membrane and the transverse colon.[7] A small uncinate process emerges from below the head, situated behind the superior mesenteric vein and sometimes artery.[7]

The neck of the pancreas separates the head of the pancreas, located in the curvature of the duodenum, from the body. The neck is about 2 cm (0.79 in) wide, and sits in front of where the portal vein is formed. The neck lies mostly behind the pylorus of the stomach, and is covered with peritoneum. The anterior superior pancreaticoduodenal artery travels in front of the neck of the pancreas.[7]

The body is the largest part of the pancreas, and mostly lies behind the stomach, tapering along its length. The peritoneum sits on top of the body of the pancreas, and the transverse colon in front of the peritoneum.[7] Behind the pancreas are several blood vessels, including the aorta, the splenic vein, and the left renal vein, as well as the beginning of the superior mesenteric artery.[7] Below the body of the pancreas sits some of the small intestine, specifically the last part of the duodenum and the jejunum to which it connects, as well as the suspensory ligament of the duodenum which falls between these two. In front of the pancreas sits the transverse colon.[8]

The pancreas narrows towards the tail, which sits near to the spleen.[7] It is usually between 1.3–3.5 cm (0.51–1.38 in) long, and sits between the layers of the ligament between the spleen and the left kidney. The splenic artery and vein, which also passes behind the body of the pancreas, pass behind the tail of the pancreas.[7]

Blood supply

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The pancreas has a rich blood supply, with vessels originating as branches of both the coeliac artery and superior mesenteric artery.[7] The splenic artery, the largest branch of the celiac trunk, runs along the top of the pancreas, and supplies the left part of the body and the tail of the pancreas through its pancreatic branches, the largest of which is called the greater pancreatic artery.[7] The superior and inferior pancreaticoduodenal arteries run along the back and front surfaces of the head of the pancreas adjacent to the duodenum. These supply the head of the pancreas. These vessels join together (anastamose) in the middle.[7]

The body and neck of the pancreas drain into the splenic vein, which sits behind the pancreas.[7] The head drains into, and wraps around, the superior mesenteric and portal veins, via the pancreaticoduodenal veins.[7]

The pancreas drains into lymphatic vessels that travel alongside its arteries, and has a rich lymphatic supply.[7] The lymphatic vessels of the body and tail drain into splenic lymph nodes, and eventually into lymph nodes that lie in front of the aorta, between the coeliac and superior mesenteric arteries. The lymphatic vessels of the head and neck drain into intermediate lymphatic vessels around the pancreaticoduodenal, mesenteric and hepatic arteries, and from there into the lymph nodes that lie in front of the aorta.[7]

Microanatomy

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This image shows a pancreatic islet when pancreatic tissue is stained and viewed under a microscope. Parts of the digestive ("exocrine") pancreas can be seen around the islet, more darkly. These contain hazy dark purple granules of inactive digestive enzymes (zymogens).

A pancreatic islet that uses fluorescent antibodies to show the location of different cell types in the pancreatic islet. Antibodies against glucagon, secreted by alpha cells, show their peripheral position. Antibodies against insulin, secreted by beta cells, show the more widespread and central position that these cells tend to have.[9]

The pancreas contains tissue with an endocrine and exocrine role, and this division is also visible when the pancreas is viewed under a microscope.[10]

The majority of pancreatic tissue has a digestive role. The cells with this role form clusters (Latin: acini) around small ducts, and are arranged in lobes that have thin fibrous walls. The cells of each acinus secrete inactive digestive enzymes called zymogens into the small intercalated ducts which they surround. In each acinus, the cells are pyramid-shaped and situated around the intercalated ducts, with the nuclei resting on the basement membrane, a large endoplasmic reticulum, and a number of zymogen granules visible within the cytoplasm. The intercalated ducts drain into larger intralobular ducts within the lobule, and finally interlobular ducts. The ducts are lined by a single layer of column-shaped cells. There is more than one layer of cells as the diameter of the ducts increases.[10]

The tissues with an endocrine role within the pancreas exist as clusters of cells called pancreatic islets (also called islets of Langerhans) that are distributed throughout the pancreas.[9] Pancreatic islets contain alpha cells, beta cells, and delta cells, each of which releases a different hormone. These cells have characteristic positions, with alpha cells (secreting glucagon) tending to be situated around the periphery of the islet, and beta cells (secreting insulin) more numerous and found throughout the islet.[9] Enterochromaffin cells are also scattered throughout the islets.[9] Islets are composed of up to 3,000 secretory cells, and contain several small arterioles to receive blood, and venules that allow the hormones secreted by the cells to enter the systemic circulation.[9]

Variation

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The size of the pancreas varies considerably.[7] Several anatomical variations exist, relating to the embryological development of the two pancreatic buds. The pancreas develops from these buds on either side of the duodenum. The ventral bud rotates to lie next to the dorsal bud, eventually fusing. In about 10% of adults, an accessory pancreatic duct may be present if the main duct of the dorsal bud of the pancreas does not regress; this duct opens into the minor duodenal papilla.[11] If the two buds themselves, each having a duct, do not fuse, a pancreas may exist with two separate ducts, a condition known as a pancreas divisum. This condition has no physiologic consequence.[12] If the ventral bud does not fully rotate, an annular pancreas may exist, where part or all of the duodenum is encircled by the pancreas. This may be associated with duodenal atresia.[13]

Gene and protein expression

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Further information: Bioinformatics § Gene and protein expression

10,000 protein coding genes (~50% of all human genes) are expressed in the normal human pancreas.[14][15] Less than 100 of these genes are specifically expressed in the pancreas. Similar to the salivary glands, most pancreas-specific genes encode for secreted proteins. Corresponding pancreas-specific proteins are either expressed in the exocrine cellular compartment and have functions related to digestion or food uptake such as digestive chymotrypsinogen enzymes and pancreatic lipase PNLIP, or are expressed in the various cells of the endocrine pancreatic islets and have functions related to secreted hormones such as insulin, glucagon, somatostatin and pancreatic polypeptide.[16]

Development

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The pancreas originates from the foregut, a precursor tube to part of the digestive tract, as a dorsal and ventral bud. As it develops, the ventral bud rotates to the other side and the two buds fuse together.

The pancreas forms during development from two buds that arise from the duodenal part of the foregut, an embryonic tube that is a precursor to the gastrointestinal tract.[11] It is of endodermal origin.[11] Pancreatic development begins with the formation of a dorsal and ventral pancreatic bud. Each joins with the foregut through a duct. The dorsal pancreatic bud forms the neck, body, and tail of the developed pancreas, and the ventral pancreatic bud forms the head and uncinate process.[11]

The definitive pancreas results from rotation of the ventral bud and the fusion of the two buds.[11] During development, the duodenum rotates to the right, and the ventral bud rotates with it, moving to a position that becomes more dorsal. Upon reaching its final destination, the ventral pancreatic bud is below the larger dorsal bud, and eventually fuses with it. At this point of fusion, the main ducts of the ventral and dorsal pancreatic buds fuse, forming the main pancreatic duct. Usually, the duct of the dorsal bud regresses, leaving the main pancreatic duct.[11]

Cellular development

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Pancreatic progenitor cells are precursor cells that differentiate into the functional pancreatic cells, including exocrine acinar cells, endocrine islet cells, and ductal cells.[17] These progenitor cells are characterised by the co-expression of the transcription factors PDX1 and NKX6-1.[17]

The cells of the exocrine pancreas differentiate through molecules that induce differentiation including follistatin, fibroblast growth factors, and activation of the Notch receptor system.[17] Development of the exocrine acini progresses through three successive stages. These are the predifferentiated, protodifferentiated, and differentiated stages, which correspond to undetectable, low, and high levels of digestive enzyme activity, respectively.[17]

Pancreatic progenitor cells differentiate into endocrine islet cells under the influence of neurogenin-3 and ISL1, but only in the absence of notch receptor signaling. Under the direction of a Pax gene, the endocrine precursor cells differentiate to form alpha and gamma cells. Under the direction of Pax-6, the endocrine precursor cells differentiate to form beta and delta cells.[17] The pancreatic islets form as the endocrine cells migrate from the duct system to form small clusters around capillaries.[9] This occurs around the third month of development,[11] and insulin and glucagon can be detected in the human fetal circulation by the fourth or fifth month of development.[17]

Function

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The pancreas is involved in blood sugar control and metabolism within the body, and also in the secretion of substances (collectively pancreatic juice) that help digestion. These are divided into an "endocrine" role, relating to the secretion of insulin and other substances within pancreatic islets that help control blood sugar levels and metabolism within the body, and an "exocrine" role, relating to the secretion of enzymes involved in digesting substances in the digestive tract.[10]

Blood glucose regulation

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See also: Pancreatic islets

The pancreas maintains constant blood glucose levels (shown as the waving line). When the blood glucose level is too high, the pancreas secretes insulin and when the level is too low, the pancreas secretes glucagon.

Cells within the pancreas help to maintain blood glucose levels (homeostasis). The cells that do this are located within the pancreatic islets that are present throughout the pancreas. When blood glucose levels are low, alpha cells secrete glucagon, which increases blood glucose levels. When blood glucose levels are high beta cells secrete insulin to decrease glucose in blood. Delta cells in the islet also secrete somatostatin which decreases the release of insulin and glucagon.[9]

Glucagon acts to increase glucose levels by promoting the creation of glucose and the breakdown of glycogen to glucose in the liver. It also decreases the uptake of glucose in fat and muscle. Glucagon release is stimulated by low blood glucose or insulin levels, and during exercise.[18] Insulin acts to decrease blood glucose levels by facilitating uptake by cells (particularly skeletal muscle), and promoting its use in the creation of proteins, fats and carbohydrates. Insulin is initially created as a precursor form called preproinsulin. This is converted to proinsulin and cleaved by C-peptide to insulin which is then stored in granules in beta cells. Glucose is taken into the beta cells and degraded. The end effect of this is to cause depolarisation of the cell membrane which stimulates the release of the insulin.[18]

The main factor influencing the secretion of insulin and glucagon are the levels of glucose in blood plasma.[19] Low blood sugar stimulates glucagon release, and high blood sugar stimulates insulin release. Other factors also influence the secretion of these hormones. Some amino acids, that are byproducts of the digestion of protein, stimulate insulin and glucagon release. Somatostatin acts as an inhibitor of both insulin and glucagon. The autonomic nervous system also plays a role. Activation of Beta-2 receptors of the sympathetic nervous system by catecholamines secreted from sympathetic nerves stimulates secretion of insulin and glucagon,[19][20] whereas activation of Alpha-1 receptors inhibits secretion.[19] M3 receptors of the parasympathetic nervous system act when stimulated by the right vagus nerve to stimulate release of insulin from beta cells.[19]

Digestion

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The pancreas has a role in digestion, highlighted here. Ducts in the pancreas (green) conduct digestive enzymes into the duodenum. This image also shows a pancreatic islet, part of the endocrine pancreas, which contains cells responsible for secretion of insulin and glucagon.

The pancreas plays a vital role in the digestive system. It does this by secreting a fluid that contains digestive enzymes into the duodenum, the first part of the small intestine that receives food from the stomach. These enzymes help to break down carbohydrates, proteins and lipids (fats). This role is called the "exocrine" role of the pancreas. The cells that do this are arranged in clusters called acini. Secretions into the middle of the acinus accumulate in intralobular ducts, which drain to the main pancreatic duct, which drains directly into the duodenum. About 1.5 - 3 liters of fluid are secreted in this manner every day.[8][21]

The cells in each acinus are filled with granules containing the digestive enzymes. These are secreted in an inactive form termed zymogens or proenzymes. When released into the duodenum, they are activated by the enzyme enterokinase present in the lining of the duodenum. The proenzymes are cleaved, creating a cascade of activating enzymes.[21]

Enzymes that break down proteins begin with activation of trypsinogen to trypsin. The free trypsin then cleaves the rest of the trypsinogen, as well as chymotrypsinogen to its active form chymotrypsin.[21]

Enzymes secreted involved in the digestion of fats include lipase, phospholipase A2, lysophospholipase, and cholesterol esterase.[21]

Enzymes that break down starch and other carbohydrates include amylase.[21]

These enzymes are secreted in a fluid rich in bicarbonate. Bicarbonate helps maintain an alkaline pH for the fluid, a pH in which most of the enzymes act most efficiently, and also helps to neutralise the stomach acids that enter the duodenum.[21] Secretion is influenced by hormones including secretin, cholecystokinin, and VIP, as well as acetylcholine stimulation from the vagus nerve. Secretin is released from the S cells which form part of the lining of the duodenum in response to stimulation by gastric acid. Along with VIP, it increases the secretion of enzymes and bicarbonate. Cholecystokinin is released from Ito cells of the lining of the duodenum and jejunum mostly in response to long chain fatty acids, and increases the effects of secretin.[21] At a cellular level, bicarbonate is secreted from centroacinar and ductal cells through a sodium and bicarbonate cotransporter that acts because of membrane depolarisation caused by the cystic fibrosis transmembrane conductance regulator. Secretin and VIP act to increase the opening of the cystic fibrosis transmembrane conductance regulator, which leads to more membrane depolarisation and more secretion of bicarbonate.[22][23][24]

A variety of mechanisms act to ensure that the digestive action of the pancreas does not act to digest pancreatic tissue itself. These include the secretion of inactive enzymes (zymogens), the secretion of the protective enzyme trypsin inhibitor, which inactivates trypsin, the changes in pH that occur with bicarbonate secretion that stimulate digestion only when the pancreas is stimulated, and the fact that the low calcium within cells causes inactivation of trypsin.[21]

Additional functions

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The pancreas also secretes vasoactive intestinal peptide and pancreatic polypeptide. Enterochromaffin cells of the pancreas secrete the hormones motilin, serotonin, and substance P.[9]

Clinical significance

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Main article: Pancreatic disease

Inflammation

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Main article: Pancreatitis

Inflammation of the pancreas is known as pancreatitis. Pancreatitis is most often associated with recurrent gallstones or chronic alcohol use, with other common causes including traumatic damage, damage following an ERCP, some medications, infections such as mumps and very high blood triglyceride levels. Acute pancreatitis is likely to cause intense pain in the central abdomen, that often radiates to the back, and may be associated with nausea or vomiting. Severe pancreatitis may lead to bleeding or perforation of the pancreas resulting in shock or a systemic inflammatory response syndrome, bruising of the flanks or the region around the belly button. These severe complications are often managed in an intensive care unit.[25]

In pancreatitis, enzymes of the exocrine pancreas damage the structure and tissue of the pancreas. Detection of some of these enzymes, such as amylase and lipase in the blood, along with symptoms and findings on medical imaging such as ultrasound or a CT scan, are often used to indicate that a person has pancreatitis. Pancreatitis is often managed medically with pain reliefs, and monitoring to prevent or manage shock, and management of any identified underlying causes. This may include removal of gallstones, lowering of blood triglyceride or glucose levels, the use of corticosteroids for autoimmune pancreatitis, and the cessation of any medication triggers.[25]

Chronic pancreatitis refers to the development of pancreatitis over time. It shares many similar causes, with the most common being chronic alcohol use, with other causes including recurrent acute episodes and cystic fibrosis. Abdominal pain, characteristically relieved by sitting forward or drinking alcohol, is the most common symptom. When the digestive function of the pancreas is severely affected, this may lead to problems with fat digestion and the development of steatorrhoea; when the endocrine function is affected, this may lead to diabetes. Chronic pancreatitis is investigated in a similar way to acute pancreatitis. In addition to management of pain and nausea, and management of any identified causes (which may include alcohol cessation), because of the digestive role of the pancreas, enzyme replacement may be needed to prevent malabsorption.[25]

Cancer

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Main article: Pancreatic cancer

Pancreatic cancer, shown here, most commonly occurs as an adenocarcinoma in the head of the pancreas. Because symptoms (such as skin yellowing, pain, or itch) do not occur until later in the disease, it often presents at a later stage and has limited treatment options.

Relative incidences of various pancreatic neoplasms, with pancreatic cancers in red/pink color.[26]

Pancreatic cancers, particularly the most common type, pancreatic adenocarcinoma, remain very difficult to treat, and are mostly diagnosed only at a stage that is too late for surgery, which is the only curative treatment. Pancreatic cancer is rare in people younger than 40 and the median age of diagnosis is 71.[27] Risk factors include chronic pancreatitis, older age, smoking, obesity, diabetes, and certain rare genetic conditions including multiple endocrine neoplasia type 1, hereditary nonpolyposis colon cancer and dysplastic nevus syndrome among others.[25][28] About 25% of cases are attributable to tobacco smoking,[29] while 5–10% of cases are linked to inherited genes.[27]

Pancreatic adenocarcinoma is the most common form of pancreatic cancer, and is cancer arising from the exocrine digestive part of the pancreas. Most occur in the head of the pancreas.[25] Symptoms tend to arise late in the course of the cancer, when it causes abdominal pain, weight loss, or yellowing of the skin (jaundice). Jaundice occurs when the outflow of bile is blocked by the cancer. Other less common symptoms include nausea, vomiting, pancreatitis, diabetes or recurrent venous thrombosis.[25] Pancreatic cancer is usually diagnosed by medical imaging in the form of an ultrasound or CT scan with contrast enhancement. An endoscopic ultrasound may be used if a tumour is being considered for surgical removal, and biopsy guided by ERCP or ultrasound can be used to confirm an uncertain diagnosis.[25]

Because of the late development of symptoms, most cancer presents at an advanced stage.[25] Only 10 to 15% of tumours are suitable for surgical resection.[25] As of 2018, when chemotherapy is given the FOLFIRINOX regimen containing fluorouracil, irinotecan, oxaliplatin and leucovorin has been shown to extend survival beyond traditional gemcitabine regimens.[25] For the most part, treatment is palliative, focus on the management of symptoms that develop. This may include management of itch, a choledochojejunostomy or the insertion of stents with ERCP to facilitate the drainage of bile, and medications to help control pain.[25] In the United States pancreatic cancer is the fourth most common cause of deaths due to cancer.[30] The disease occurs more often in the developed world, which had 68% of new cases in 2012.[31] Pancreatic adenocarcinoma typically has poor outcomes with the average percentage alive for at least one and five years after diagnosis being 25% and 5% respectively.[31][32] In localized disease where the cancer is small (< 2 cm) the number alive at five years is approximately 20%.[33]

There are several types of pancreatic cancer, involving both the endocrine and exocrine tissue. The many types of pancreatic endocrine tumors are all uncommon or rare, and have varied outlooks. However the incidence of these cancers has been rising sharply; it is not clear to what extent this reflects increased detection, especially through medical imaging, of tumors that would be very slow to develop. Insulinomas (largely benign) and gastrinomas are the most common types.[34] For those with neuroendocrine cancers the number alive after five years is much better at 65%, varying considerably with type.[31]

A solid pseudopapillary tumour is a low-grade malignant tumour of the pancreas of papillary architecture that typically afflicts young women.[35]

Diabetes mellitus

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Type 1 diabetes

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Main article: Diabetes mellitus type 1

Diabetes mellitus type 1 is a chronic autoimmune disease in which the immune system attacks the insulin-secreting beta cells of the pancreas.[36] Insulin is needed to keep blood sugar levels within optimal ranges, and its lack can lead to high blood sugar. As an untreated chronic condition, complications including accelerated vascular disease, diabetic retinopathy, kidney disease and neuropathy can result.[36] In addition, if there is not enough insulin for glucose to be used within cells, the medical emergency diabetic ketoacidosis, which is often the first symptom that a person with type 1 diabetes may have, can result.[37] Type 1 diabetes can develop at any age but is most often diagnosed before age 40.[36] For people living with type 1 diabetes, insulin injections are critical for survival.[36] An experimental procedure to treat type 1 diabetes is pancreas transplantation or isolated transplantation of islet cells to supply a person with functioning beta cells.[36]

Type 2 diabetes

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Main article: Diabetes mellitus type 2

Diabetes mellitus type 2 is the most common form of diabetes.[36] The causes for high blood sugar in this form of diabetes usually are a combination of insulin resistance and impaired insulin secretion, with both genetic and environmental factors playing a role in the development of the disease.[38] Over time, pancreatic beta cells may become "exhausted" and less functional.[36] The management of type 2 diabetes involves a combination of lifestyle measures, medications if required and potentially insulin.[39] With relevance to the pancreas, several medications act to enhance the secretion of insulin from beta cells, particularly sulphonylureas, which act directly on beta cells; incretins which replicate the action of the hormones glucagon-like peptide 1, increasing the secretion of insulin from beta cells after meals, and are more resistant to breakdown; and DPP-4 inhibitors, which slow the breakdown of incretins.[39]

Removal

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It is possible for a person to live without a pancreas, provided that the person takes insulin for proper regulation of blood glucose concentration and pancreatic enzyme supplements to aid digestion.[40]

History

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The pancreas was first identified by Herophilus (335–280 BC), a Greek anatomist and surgeon.[41] A few hundred years later, Rufus of Ephesus, another Greek anatomist, gave the pancreas its name. Etymologically, the term "pancreas", a modern Latin adaptation of Greek πάγκρεας,[42] [πᾶν ("all", "whole"), and κρέας ("flesh")],[43] originally means sweetbread,[44] although literally meaning all-flesh, presumably because of its fleshy consistency. It was only in 1889 when Oskar Minkowski discovered that removing the pancreas from a dog caused it to become diabetic.[45] Insulin was later isolated from pancreatic islets by Frederick Banting and Charles Best in 1921.[45]

The way the tissue of the pancreas has been viewed has also changed. Previously, it was viewed using simple staining methods such as H&E stains. Now, immunohistochemistry can be used to more easily differentiate cell types. This involves visible antibodies to the products of certain cell types, and helps identify with greater ease cell types such as alpha and beta cells.[9]

Other animals

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Pancreatic tissue is present in all vertebrates, but its precise form and arrangement varies widely. There may be up to three separate pancreases, two of which arise from the pancreatic bud, and the other dorsally. In most species (including humans), these "fuse" in the adult, but there are several exceptions. Even when a single pancreas is present, two or three pancreatic ducts may persist, each draining separately into the duodenum (or equivalent part of the foregut). Birds, for example, typically have three such ducts.[46]

In teleost fish, and a few other species (such as rabbits), there is no discrete pancreas at all, with pancreatic tissue being distributed diffusely across the mesentery and even within other nearby organs, such as the liver or spleen. In a few teleost species, the endocrine tissue has fused to form a distinct gland within the abdominal cavity, but otherwise it is distributed among the exocrine components. The most primitive arrangement, however, appears to be that of lampreys and lungfish, in which pancreatic tissue is found as a number of discrete nodules within the wall of the gut itself, with the exocrine portions being little different from other glandular structures of the intestine.[46]

Cuisine

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The pancreas of calf (ris de veau) or lamb (ris d'agneau), and, less commonly, of beef or pork, are used as food under the culinary name of sweetbread.[47][48]

Oh my, that information is very nutritious. Thank you! :D

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punechelation1 · 1 year ago

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Difference Between Cardiac Arrest and Heart Attack – Everyone Should Know

Cardiac Arrest, Heart Attack, or a Heart Failure – Is there a difference, or are these terminologies the same? In this article, let’s focus on the difference between Cardiac Arrest and Heart attack. Here are two real-life incidences:

Situation ‘A’

Navneet was 50 years old. One morning when he was walking out of the office cafeteria, he suddenly felt a pain at the center of his chest. Navneet thought it was just a heartburn and hence kept walking. As he stopped by his friend’s desk, he got very light-headed. His friend indicated that he looked gray and insisted on calling their emergency number. However, Navneet declined and chose to walk towards his cubicle through the long corridor. His legs felt rubbery as he approached his desk, and felt so disabled that he had to cling onto the cubicle walls to get some support and remain steady. Immediately thereafter, he was admitted to the emergency room and accordingly treated.

Situation ‘B’

Suraj was in his office talking to his team member when he started to get dizzy. He started to stumble around and then ran forward straight into a door frame. He fell on the floor straight. Suraj tried to speak, but he couldn’t. He had trouble breathing and started to unbutton his shirt as he felt suffocated. He was rushed to the hospital and given a round of CPR followed by other courses of treatment.

What can be derived from the above incidences?

Navneet, while in the hospital, discovered that there was 90% occlusion in his right coronary artery and had to get a stent placed to avoid further similar occurrences; whereas in Suraj’s case, his Left Anterior Descending artery (LAD) was 100% blocked and Right Coronary Artery (RCA) was about 80% blocked.

Nevertheless, symptom-wise, both the incidents mentioned above look similar but are very different. Situation ‘A’ is a case of Heart Attack, and Situation ‘B’ is a case of Sudden Cardiac Arrest (SCA).

People assume these to be similar medical conditions and often use the terms interchangeably. However, there is a significant difference between cardiac arrest and heart attack.

Medical science has made remarkable advancements and treating a heart attack or a cardiac arrest is much more possible, even non-surgically. Poona Preventive Cardiovascular Centre (PPCC) offers the most viable non-surgical treatment in Pune for heart diseases with the best and safest modern techniques. We solely believe in delivering scientifically-validated therapeutics for healthy and long-term wellbeing.

Since heart attack or cardiac arrest episodes can be fatal and traumatic, causing a high degree of damage to the heart anyway, it is always advisable that, if possible, you must opt for non-surgical treatment to go mild and easy on your heart.

To understand the major difference between Cardiac Arrest and Heart Attack, first, let’s get to know what these conditions are like?

What happens in a Heart attack?

Your heart beats 60 to 100 times a minute due to the oxygen that it carries. An instance of Heart attack can occur when a layer of plaque, a combination of cholesterol, fat, and other substances, blocks the oxygen-borne blood flow to the heart muscles.

What signs indicate a Heart Attack?

Usually, heart attack symptoms gradually begin developing a few hours, days, or weeks earlier and persist for some time. Also, the heart does not stop beating during a heart attack even after the blood supply is disrupted. Moreover, symptoms of heart attack can differ in men and women.

Few noticeable symptoms during a heart attack:

Pressure, tightness, pain, squeezing, or aching sensations in your chest or arms, which may spread to your neck, jaw, or back

Symptoms such as nausea, indigestion, heartburn, or abdominal pain may also be seen

Breathing difficulty

Cold sweat

Fatigue

Light-headedness or dizziness that may occur suddenly

Does your heart get damaged after a heart attack?

The heart is a very sturdy organ. So, after suffering an attack, even though some of it may get damaged, the other half keeps functioning. But, your heart may come down to a weakened condition that might need greater care after that.

What happens in a Cardiac Arrest?

Sudden Cardiac Arrest (SCA) may occur when there is a sudden loss of heart function. Due to irregular heartbeat (arrhythmia), the pumping action is disturbed, and the heart is unable to supply blood to the brain, lungs, and other parts of the body. Within a few seconds, the person falls unconscious, having no pulse. Untreated, such a condition worsens and leads to death.

It can happen to anyone at any time, although it most often happens in people already having some other health problem or who have a heart condition. The most common cause of a cardiac arrest is ventricular fibrillation, which happens when the electrical impulses tell your heart to beat.

Further SCA symptoms that show the difference between Cardiac Arrest and Heart Attack:

Sudden cardiac arrest symptoms are immediate and severe, including:

Unexpected collapse

No pulse detected

No breathing.

Unconsciousness

Few other signs and symptoms may appear prior to a sudden cardiac arrest. These could include:

Chest ache

Weakness due to shortness of breath

Palpitations are symptoms of a fast-beating, fluttering, or pounding heart. However, sudden cardiac arrest often occurs without warning.

Is there a link between SCA and Heart Attack?

Although medically, there is a wide difference between Cardiac Arrest and Heart Attack, these two conditions are interlinked. Basically, a heart attack may turn out to be the onset of a cardiac arrest as SCA may occur post a heart attack or while recovering from one. We can also say that heart attack may be a common cause of cardiac arrest.

Apart from a heart attack, thickened heart muscle, arrhythmias, ventricular fibrillation, and long Q-T syndrome can also be the reasons for a Sudden Cardiac Arrest.

Cardiac Arrest Vs Heart Attack – In a nutshell

Cardiac Arrest

Heart attack

Sudden cardiac arrest is typically a medical emergency that can happen after the heart suddenly stops beating.

On the other hand, heart attack refers to a more serious condition in which a clogged artery interrupts blood from flowing to the heart.

When a person’s heart stops pumping blood around their body, he stops breathing normally. In such a case, the person is said to be under cardiac arrest.

A heart attack is the cause of many cardiac arrests in adults. This is because a person experiencing a heart attack may develop a dangerous heart rhythm, resulting in cardiac arrest.

What steps should you take during a heart attack or a cardiac arrest?

Although there is a difference between Cardiac Arrest and Heart Attack, the emergency care steps could be similar:

Call the nearest medical emergency available

Start CPR straight away

Make sure there is room to lay down next to the person

Place your hands on the middle of the person’s chest

Push hard and fast in a downward motion at least 100 times.

Then, continue to push hard and fast for another 100 compressions

If you are on the floor, place your hands on the person’s shoulder to tilt their head back

Continue the CPR process until professional emergency arrives.

We are proud to hone the fact that Poona Preventive Cardiovascular Center (PPCC) is the only clinic in Pune to be specialized in modern science techniques like Chelation Therapy, EECP, ESMR, and HBOT, ensuring effective non-surgical treatment in Pune for heart problems. We are completely dedicated to efficient management of Cardiovascular diseases and heart disorders to avoid risky surgeries. With tailored programs comprising lifestyle modification, diet management, and nutritional supplements, we make sure that our patients are healthy and hearty for a long time.

#alternative to bypass surgery #esmr treatment in pune #eecp treatment in pune #poona preventive #alternative to bypass #EECP treatment #ESMR treatment

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cardiologybd · 1 year ago

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A Case Report of Tetralogy of Fallot Associated with Tight Lesion of the Left Anterior Descending Coronary Artery

Read the full article

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sandeep-health-care · 1 year ago

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KEEP CALM AND RECONSIDER GRAFT REVISION

Preoperative angiography in combination with intraoperative graft flow measurements may improve durability of coronary artery bypass grafts. However, native coronary flow might impair bypass graft flow based on stenoses’ severity, leading to inferior long-term outcomes. Intraoperative routine snaring of a coronary artery detects significant competitive flow, possibly intercepting unnecessary perioperative graft revisions.

The heart, inadequate blood supply, and revascularisation The coronary arteries supply the heart itself with oxygen and nutrients. Severe narrowing of these coronaries (stenosis) might lead to chest pain or a heart attack. Myocardial revascularisation by either percutaneous coronary intervention or coronary artery bypass graft (CABG) improves symptoms, quality of life and survival in these patients. A stenosis with a diameter reduction < 50 per cent is considered a mild stenosis, 50 – 70 per cent as moderate, and > 70 per cent as severe. Unfortunately, the degree of coronary stenosis can easily be overestimated and impacts short and long-term outcomes of CABG.

A heart lung machine takes over the heart’s pumping function and gas transfer of the lungs during heart surgery. Major drawbacks, however, are a systemic inflammatory response, acute kidney injury or brain infarctions. For CABG, the heart lung machine can be abandoned by performing off-pump coronary artery bypass grafting where the heart keeps beating during surgery.

Intraoperative choices and challenges lead to postoperative complications Patients’ own arteries from the chest or lower arm can be used to create these coronary bypasses. These arterial grafts have excellent long-term functionality, and low redo revascularisation rates. Arterial grafts require proper handling to avoid early technical failure. Competitive flow from native coronaries that are not narrowed enough impacts long term success of the coronary bypass. Detection of competitive flow for arterial grafts as early as possible after making the anastomosis might predict the longterm patency.

Intraoperative assessment of graft flow can be measured with transit time flow measurements (TTFM). European guidelines on myocardial revascularisation suggest routine use of intraoperative bypass graft flow assessment. Unfortunately, this quality control technique is not always used, nor handled upon adequately during surgery. The first signs of a failed graft are heart rhythm changes, postoperative new onset of chest pain and a potential myocardial infarction might occur. Often, the patient already left the operating theatre, and bypass graft revision is not possible, or should be considered for another surgical procedure.

Cut-off values for TTFM to indicate graft failure are still debated, and are not uniform between clinical studies. In a recent study conducted at Thoraxcentrum Twente of Medisch Spectrum Twente (Netherlands), preoperative angiography findings were combined with intraoperative TTFM in 50 CABG patients without the use of a heart lung machine (off-pump CABG). All patients had significant coronary artery disease as established by heart team discussion between a cardiologist and heart surgeon.

Temporary closing of a severely narrowed coronary artery During off-pump CABG, a bypass graft was made with the left internal thoracic artery (LIMA) on the largest coronary artery on the front side of the heart (left anterior descending artery, LAD). This coronary artery was then temporarily closed and the bypass graft flow was measured with TTFM. Hereafter, a new measurement was performed with the coronary artery reopened. After the initial bypass graft, arterial grafts were placed to other parts of the heart.

As expected, higher values of bypass graft flow were observed with the coronary artery snared, effectively preventing any competitive flow. More interestingly, the mean graft flow increased from 20 mL/min with open LAD to 30 mL/min with snared LAD and differed between severity of coronary stenosis groups (Figure 1). In more than half of the patients (52 per cent) the mean graft flow was lower than clinical relevant TTFM cut-off values with the LAD open. Graft flow increased in 16 patients after snaring the LAD, and shifted to acceptable TTFM values. This increase might indicate an open, and functional anastomosis affected by competitive flow from the native coronary artery. Here, surgical graft revision will not likely improve baseline TTFM values such as mean graft flow or graft patency, resulting in a useless or even harmful procedure.

Is snaring safe? Snaring the LAD is a widespread method to obtain a bloodless operative field, and is well tolerated by patients. Indeed, this technique is comparable to intracoronary shunting regarding postoperative heart enzyme rise. Atherosclerotic plaques or calcified coronary arteries make shunting technically more tough. Prolonged snaring might induce blood vessel injury, and arrhythmias, but are reversible up to 20-30 minutes of snaring.

Patient-specific decision making before and during surgery Patient-specific decision making is performed daily in heart team discussion between cardiac surgeons and cardiologists according to international guidelines. Here patient characteristics determine decision making for a surgical, percutaneous or conservative treatment. Combining patient characteristics with procedural characteristics could further tailor treatment and thus improve outcomes for patients.

Professional information for decision making is scattered. Direct comparison between competing treatments or diagnosis modalities is often lacking. For assessing coronary artery stenosis, visual eyeballing by a cardiologist is most common, although high intra-and inter-observer variability exists for many years with low concordance around clinical relevant cut-off points. Some centres use quantitative coronary analysis (QCA) with 2D or 3D reconstruction using cardiac angiography to analyse degree of stenosis for research purposes, but are rarely used for heart team discussions. To predict graft patency, it is no match compared to functional assessment using the more invasive fractional flow reserve (FFR). Here, clinical cut-off values are also debated and might even differ between percutaneous coronary intervention or CABG. Future studies should investigate the cut-off values of FFR or QCA for PCI and CABG to optimise outcome for patients.

Read More: https://www.europeanhhm.com/medical-sciences/keep-calm-and-reconsider-graft-revision

#doctors #health and wellness #healthy lifestyle #medical equipment #medical care #technologies #health #healthcare #hospitals #medical science #graft version

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heartheathblogs · 3 months ago

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Understanding the Anterior Interventricular Artery: A Key Player in Heart Health

The Anterior Interventricular Artery (AIA), often referred to as the Left Anterior Descending (LAD) artery, plays a critical role in maintaining heart health. It is one of the main branches of the left coronary artery, running down the front of the heart along the interventricular septum, the wall separating the left and right ventricles.

This artery is responsible for supplying oxygen-rich blood to a significant portion of the heart muscle, particularly the front and lower parts of the left ventricle and the septum. Given its essential function, any blockage or narrowing in the AIA can have serious consequences, potentially leading to conditions such as angina, heart attacks, or other forms of coronary artery disease.

The LAD is sometimes called the "widow-maker" artery because blockages here are often fatal without prompt medical intervention. Understanding the anatomy and importance of the Anterior Interventricular Artery underscores the need for maintaining heart health through regular check-ups, a balanced diet, and a healthy lifestyle. This knowledge is vital for both medical professionals and individuals in preventing and managing heart disease effectively.

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lupine-publishers-juns · 1 year ago

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Lupine Publishers | Briefly about The Ureter

Abstract

Every man has two kidneys. Each kidney has a ureter, which drains urine from a central collection point into the bladder. From the bladder, urine is excreted through the urethra from the body through the penis in men and the vulva in women. The most important role of the kidneys is to filter metabolic waste products and excess salt and water from the body and help remove them from the body. The kidneys also help regulate blood pressure and make red blood cells.

Keywords: Kidney; Obstruction; UTI; Injury

Introduction

The ureters are tubular structures responsible for the transportation of urine from the kidneys to the bladder. The length ranges from 22 to 30 cm, and they have a wall made up of multiple layers. The innermost layer is made up of transitional epithelium, surrounded by the lamina propria, which is a connective tissue layer. These two layers make up the mucosal lining. The next layer is made of smooth muscle that, as mentioned previously, is continuous with that of the calyces and the renal pelvis. However, one slight difference is that within the ureter, the smooth muscle layer is divided into an inner longitudinal and an outer circular layer. These muscular layers allow peristalsis of urine. The outermost layer is the adventitia, which is a thin layer enveloping the ureter, its blood vessels, and lymphatics. The ureter is often divided into three segments: the upper (proximal), middle, and lower (distal) segments. The upper segment starts from the renal pelvis to the upper border of the sacrum. The middle segment is the part between the upper border and lower border of the sacrum. The lower segment is from the lower border of the sacrum to the bladder.

Anatomy

Each ureter lies posterior to the renal artery and vein at the ureteropelvic junction [1]. They then descend anterior to the psoas major muscle and the ilioinguinal nerves, just anterior to the tips of the lumbar transverse vertebral processes. Approximately a third of the way down, the ureters are crossed by the gonadal vessels. They then cross the bifurcated common iliac arteries and run along the anterior border of the internal iliac artery toward the bladder, which it pierces in an oblique manner. It is this oblique entry of the ureter into the bladder, the intramural segment of the ureter that acts as a nonreturn valve preventing vesicoureteric reflux. This valve can be congenitally defective such as that seen in those with short intramural segments, or rendered ineffective as a result of injury, such as surgery or disease, all of which leads to reflux. Many congenital abnormalities of this oblique tunnel are seen in association with a duplex kidney and ureterocoele. In its lower third, the ureters pass posterior to the superior vesical branch of the internal iliac artery also called ‘umbilical artery’. On the right side, the ureter is related anteriorly to the second part of the duodenum, caecum, appendix, ascending colon, and colonic mesentery. The left ureter is closely related to the duodenojejunal flexure of Treitz, descending and sigmoid colon, and their mesenteries.

Obstruction

The diagnosis of obstruction cannot be made on the basis of haematological or biochemical tests [2]. There may be evidence of impaired renal function, anaemia of chronic disease, haematuria or bacteriuria in selected cases. Ultrasonography is a reliable means of screening for upper urinary tract dilatation. Ultrasound cannot distinguish a baggy, low-pressure, unobstructed system from a tense, high pressure, obstructed one, so that falsepositive scans are seen. A normal scan usually but not invariably rules out urinary tract obstruction. If obstruction is intermittent or in its very early stages, or if the pelvicalyceal system cannot dilate owing to compression of the renal substance, for example by tumour, the ultrasound scan may fail to detect the problem. Radionuclide studies may be helpful. If obstruction has resulted in prolongation of the time taken for urine to travel down the renal tubules and collecting system (obstructive nephropathy) this can be detected by nuclear medicine techniques and is diagnostic. Conversely, in the presence of a baggy, low-pressure, unobstructed renal pelvis and calyceal system, nephron transit time will be normal, but pelvic transit time prolonged. If doubt exists, frusemide may be administered; satisfactory ‘washout’ of radionuclide rules out obstruction and vice versa. Relative uptake of isotope may be normal or reduced on the side of the obstruction and peak activity of the isotope may be delayed. In general, absence of uptake of radiopharmaceutical indicates renal damage sufficiently severe to render correction of obstruction unprofitable. Isotope studies may thus provide a guide to the form of surgery to be undertaken. Antegrade pyelography and ureterography are extremely useful in defining the site and cause of obstruction and can be combined with drainage of the collecting system by percutaneous needle nephrostomy. The risk of introducing infection is less than with retrograde ureterography in which technique instrumentation of the bladder is followed by injection of contrast into the lower ureter or ureters. This technique is indicated if antegrade examination cannot be carried out for some reason or if there is a possibility of dealing with ureteric obstruction from below at the time of examination. Ureteral obstruction occurs in 2–10% of renal transplants and often manifests itself as painless impairment of graft function due to the lack of innervation of the engrafted kidney [3]. Hydronephrosis may be minimal or absent in early obstruction, whereas low-grade dilatation of the collecting system secondary to edema at the ureterovesical anastomosis may be seen early post-transplantation and does not necessarily indicate obstruction. A full bladder may also cause mild calyceal dilatation due to ureteral reflux and repeat ultrasound with an empty bladder should be carried out. Persistent or increasing hydronephrosis on repeat ultrasound examinations is highly suggestive of obstruction. Renal scan with furosemide washout may help support the diagnosis, but it does not provide anatomic details. Confirmation of the obstruction can be made by retrograde pyelogram but the ureteral orifice may be difficult to catheterize. Although invasive, percutaneous nephrostomy tube placement with antegrade nephrostogram is the most effective way to visualize the collecting system and can be of both diagnostic and therapeutic value.

Blood clots, technically poor reimplant, and ureteral sloughing are common causes of early acute obstruction after transplantation. Ureteral fibrosis secondary to either ischemia or rejection can cause intrinsic obstruction. The distal ureter close to the ureterovesical junction is particularly vulnerable to ischemic damage due to its remote location from the renal artery, hence compromised blood supply. Although uncommon, ureteral fibrosis associated with polyoma BK virus in the setting of renal transplantation has been well-described. Ureteral kinking, lymphocele, pelvic hematoma or abscess, and malignancy are potential causes of extrinsic obstruction. Calculi are uncommon causes of ureteral obstruction. Definitive treatment of ureteral obstruction due to ureteral strictures consists of either endourologic techniques or open surgery. Intrinsic ureteral scars can be treated effectively by endourologic techniques in an antegrade or retrograde approach. An indwelling stent may be placed to bypass the ureteral obstruction and removed cystoscopically after 2–6 weeks. An antegrade nephrostogram should be performed to confirm that the urinary tract is unobstructed prior to nephrostomy tube removal. Routine ureteral stent placement at the time of transplantation has been suggested to be associated with a lower incidence of early postoperative obstruction. Extrinsic strictures, strictures that are longer than 2 cm, or those that have failed endourologic incision, are less likely to be amenable to percutaneous techniques and are more likely to require surgical intervention. Obstructing calculi can be managed by endourologic techniques or by extracorporeal shock wave lithotripsy.

UTI

Urinary tract infections (UTIs) are the most common bacterial infection in the paediatric population [4]. The incidence is initially higher in boys, affecting up to 20.3% of uncircumcised boys and 5% of girls at the age of 1. There is a gradual shift, with UTIs affecting 3% of prepubertal girls and 1% of prepubertal boys. The National Institute for Health and Care Excellence (NICE) have defined a recurrent UTI as two or more episodes of pyelonephritis, or one episode of pyelonephritis plus one or more episodes of cystitis, or three or more episodes of cystitis. Diagnostic investigations include urinalysis, which may require suprapubic bladder aspiration or bladder catheterisation in infants. A urine culture and microscopy should be carried out if there is evidence of infection. The role of further imaging is to differentiate between an uncomplicated and complicated UTI, but should also be considered in those with haematuria. A UTI is complicated in the presence of an abnormal urinary tract including upper tract dilatation, atrophic or duplex kidneys, ureterocoele, posterior urethral valves, intestinal connections, and vesico-ureteric reflux (VUR). NICE guidelines recommend an urgent ultrasound of the urinary tract for all those with recurrent UTI under six months. For children six months and older, NICE in the UK recommends an ultrasound within six weeks of the latest infective episode. All children with recurrent UTIs should be referred to a paediatric specialist and have a dimercaptosuccinic acid (DMSA) scan within four to six months of an acute infection to evaluate for renal scarring. European Association of Urology (EAU) guidelines recommend a renal tract ultrasound in febrile UTIs if there is no clinical improvement, as an abnormal result is seen in 15% of these patients. Routinely repeating a urine culture in children treated with an antibiotic based on previous urine culture susceptibilities is not necessary [5]. Approximately 10%–30% of children develop at least one recurrent UTI, and the recurrence rate is highest within the first 3 to 6 months after a UTI. Renal scarring increases with an increasing number of febrile UTIs and with delayed treatment; therefore, parents should be counseled regarding the high risk of recurrent UTI and seek prompt evaluation for subsequent febrile illnesses in their child. Children who had a febrile UTI should routinely have their height, weight, and blood pressure monitored by their primary care provider. Children with significant bilateral renal scars or a reduction of renal function warrant long-term follow-up for the assessment of hypertension, renal function, and proteinuria.

Colic

Urolithiasis represents the commonest cause of acute ureteric colic, with calcium stones accounting for approximately 80% of cases [6]. Ureteric calculi have a prevalence of approximately 2–3% in Caucasian populations, with a lifetime risk of 10–12% in males and 5–6% in females. They are more common in developed countries, in men, in those with a positive family history, and in those with inadequate daily water intake. Ureteric colic typically presents with acute severe loin pain – which patients often describe as unrelenting despite a number of postural changes – and haematuria. Vomiting is often a feature of severe uncontrolled pain. Most patients with renal colic present because of severe uncontrolled pain and do not have signs of overt sepsis. Opiates are commonly given, although diclofenac sodium has been shown to be at least as effective for pain relief, particularly via rectal administration. Despite initial concerns, diclofenac sodium therapy has not been associated with renal toxicity in patients with preexisting normal renal function. Fever, tachycardia, tachypnoea and hypotension suggest sepsis secondary to an infected, obstructed kidney, which represents a life-threatening condition. Immediate management comprises prompt resuscitation, establishment of intravenous (IV) antibiotics, rapid diagnosis and decompression of the obstructed renal system, usually by ultrasound-guided percutaneous nephrostomy. Early involvement of urology and critical care services is essential in such patients. The management of ureteric calculi depends upon factors relating to the stone and the patient. Pre-eminent stone factors are size and site. It has been shown that 71–98% of stones <5 mm will pass spontaneously, whereas rates of spontaneous passage for stones >7 mm are low. Stone passage is also related to location in the ureter; 25% of proximal, 45% of mid and 75% of distal ureteric stones will pass spontaneously. In patients in whom stone passage is deemed likely, a trial of conservative management should be employed. Exceptions include patients with a functional or anatomical solitary kidney, bilateral ureteric obstruction, uncontrolled pain, or the presence of infection. Patients without contraindications should receive diclofenac sodium 50 mg tds, which has been shown to reduce the frequency of recurrent renal colic episodes. Recent evidence suggests that additional treatment with smooth muscle relaxants is associated with increased rates of stone passage over analgesics alone. A recent meta-analysis of studies using either nifedipine or tamsulosin, showed an approximate 65% greater chance of stone passage when such agents were used compared with equivalent controls. Intervention is generally reserved for large stones (>7 mm), conservative treatment failures and those with contraindications to a watchful waiting approach. Options include extracorporeal shockwave lithotripsy and retrograde ureteroscopic stonefragmentation.

A stone can traverse the ureter without symptoms, but passage usually produces pain and bleeding [7]. The pain begins gradually, usually in the flank, but increases over the next 20–60 min to become so severe that narcotics may be needed for its control. The pain may remain in the flank or spread downward and anteriorly toward the ipsilateral loin, testis, or vulva. A stone in the portion of the ureter within the bladder wall causes frequency, urgency, and dysuria that may be confused with urinary tract infection. The vast majority of ureteral stones <0.5 cm in diameter pass spontaneously. Helical computed tomography (CT) scanning without radiocontrast enhancement is now the standard radiologic procedure for diagnosis of nephrolithiasis. The advantages of CT include detection of uric acid stones in addition to the traditional radiopaque stones, no exposure to the risk of radiocontrast agents, and possible diagnosis of other causes of abdominal pain in a patient suspected of having renal colic from stones. Ultrasound is not as sensitive as CT in detecting renal or ureteral stones. Standard abdominal x-rays may be used to monitor patients for formation and growth of kidney stones, as they are less expensive and provide less radiation exposure than CT scans. Calcium, cystine, and struvite stones are all radiopaque on standard x-rays, whereas uric acid stones are radiolucent.

Ureteral Stone Disease

Nephrolithiasis occurs with an estimated overall prevalence of 5.2% and there is evidence that stone disease is on the rise [8]. However, many stones in the kidney go undetected because they cause no symptoms or obstruction. Conversely, ureteral stones rarely remain silent, and they have greater potential for causing pain and obstruction. As such, ureteral stones that fail to pass spontaneously require surgical intervention. Although the introduction of medical expulsive therapy (MET, the use of pharmacological agents to promote spontaneous stone passage) has changed the natural history of ureteral stone disease, not all ureteral stones respond to MET. Indications for surgical intervention to remove ureteral calculi include stones that are unlikely or fail to pass spontaneously with or without MET, stones that cause unremitting pain regardless of the likelihood of spontaneous passage, stones associated with persistent, high-grade obstruction, stones in patients with an anatomically or functionally solitary kidney or in those with renal insufficiency or stones in patients for whom their occupation or circumstances mandate prompt resolution (i.e. pilots, frequent travelers, etc.). Once the decision has been made to intervene surgically for a patient with a ureteral stone, treatment options include shock-wave lithotripspy, ureteroscopy, percutaneous antegrade ureteroscopy and open or laparoscopic ureterolithotomy. Although special cirumstances may dictate the application of percutaneous antegrade ureteroscopy or ureterolithotomy (large, impacted stones, stones in patients with urinary diversions or stones that fail less invasive approaches), the two most widely practiced treatment modalities for ureteral stones are shock-wave lithotripsy (SWL) and ureteroscopy (URS). Both are associated with high success rates and low morbidity. However, the optimal treatment for ureteral stones remains controversial because of passionate advocates on both sides of the controversy. Proponents of SWL cite the noninvasiveness, high patient satisfaction and ease of treatment, while URS advocates favor the short operative times, high success rates and short time interval to become stone free.

Cystoscopy

Cystoscopic examination of urethra and bladder should be systematic [9]. The female urethra is only 2.5–4 cm long. Urethral mucosa should be examined for strictures, diverticular opening, or polyps, and the bladder neck is visualised as scope enters and exits the bladder. Base and trigone of the bladder are initially inspected. Trigone lies proximal to the bladder neck; it is the triangular area bounded by the inter-ureteric ridge and the bladder neck at the base of the bladder. One of the most common features of the trigone is squamous metaplasia, present in up to 50% of the women. It is a benign feature with no malignant potential. In staging for cervical cancer, when imaging suggests stage 3 or 4 disease, cystoscopy is indicated. The bladder base and trigone appearance such as bullous edema, inflammatory changes, or infiltration has to be documented, and in case of infiltration, biopsy should be part of the evaluation. Ureteric orifices are slit-like openings easily identifiable by the presence of efflux on either side of the inter-ureteric ridge. The ureteral orifices location, number, nature of ureteric efflux (clear, blood stained), and any anatomical distortion is noted. In a woman with anterior vaginal wall prolapse or an underlying cervical mass, identification of trigone or ureteric orifices may be difficult. In such cases, placing a finger inside the vagina and elevating the bladder base with a finger will be helpful. Blood stained ureteric efflux denotes upper tract pathology and further assessment of the ureter and kidneys is indicated, either by ultrasound or a CT scan of the kidneys, ureters, and bladder (CT KUB). In intra-operative or postoperative ureteral integrity assessment, presence of just ureteric peristalsis does not rule out ureteral injury. Checking for ureteric efflux after administration of methylthionium chloride or indigo carmine (5ml) IV is effective in confirming ureteral patency.

Injury

Most ureteral injuries are iatrogenic in the course of pelvic surgery [10]. Ureteral injury may occur during transurethral bladder or prostate resection or ureteral manipulation for stone or tumor. Ureteral injury is rarely a consequence of penetrating trauma. Unintentional ureteral ligation during operation on adjacent organs may be asymptomatic, though hydronephrosis and loss of renal function results. Ureteral division leads to extravasation and urinoma. If the ureteral injury is not recognized at surgery, the patient may complain of flank and lower abdominal pain on the injured side. Ileus and pyelonephritis may develop. Later, urine may drain through the wound (or through the vagina following transvaginal surgery) or there may be increased output through a surgical drain. Wound drainage may be evaluated by comparing creatinine levels found in the drainage fluid with serum levels; urine exhibits very high creatinine levels when compared with serum. Intravenous administration of 5 mL of indigo carmine causes the urine to appear blue-green; therefore, drainage from an ureterocutaneous fistula becomes blue, compared to serous drainage. Anuria following pelvic surgery not responding to intravenous fluids may rarely signify bilateral ureteral ligation or injury. Peritoneal signs may occur if urine leaks into the peritoneal cavity.

Conclusion

The ureter starts from the renal pelvis, descends down the retroperitoneal space of the abdominal cavity and enters the pelvis, where it ends by pouring into the urinary bladder. Therefore, it distinguishes the abdominal and pelvic part. The boundary between these parts is the so-called terminal line. When entering the pelvic cavity, the ureter forms a border curve and in this narrowed part the kidney stone can be stopped. The curvature of the ureter is projected on the anterior abdominal wall in the area of the Hale topographic point. Urinary tracts pass through the bladder wall obliquely. When the bladder wall is stretched, the fold of its mucosa acts as a valve and prevents the return of urine to the ureters and the possible spread of infection from the bladder to the kidneys.

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